{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T23:56:59Z","timestamp":1792799819914,"version":"4.5.0"},"reference-count":25,"publisher":"SAGE Publications","issue":"8","license":[{"start":{"date-parts":[[2024,4,15]],"date-time":"2024-04-15T00:00:00Z","timestamp":1713139200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"name":"Japanese MEXT (The Ministry of Education, Culture, Sports, Science and Technology) KAKENHI","award":["20K08810"],"award-info":[{"award-number":["20K08810"]}],"id":[{"id":"https:\/\/ror.org\/048rj2z13","id-type":"ROR","asserted-by":"crossref"}]}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Lupus"],"published-print":{"date-parts":[[2024,7]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>This study aimed to investigate the role of the programmed cell death protein 1 (PD-1) pathway and T peripheral helper (Tph) cells in the pathogenesis of lupus nephritis using lupus-prone BXSB- Yaa mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Male BXSB- Yaa mice and age-matched male C57BL\/6 mice were used. The expression of PD-1 and its ligands (programmed cell death 1 ligand-1, PD-L1 and programmed cell death 1 ligand-2, PD-L2) and the phenotypes of kidney-derived cells and splenocytes expressing these molecules were analyzed by immunofluorescence and flow cytometry.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Nephritis spontaneously developed in 16-week-old but not in 8-week-old BXSB- Yaa or C57BL\/6 mice. PD-1 was expressed on CD4\n                      <jats:sup>+<\/jats:sup>\n                      mononuclear cells (MNCs) that infiltrated the glomeruli of 16-week-old BXSB- Yaa mice. The frequency of CD4\n                      <jats:sup>+<\/jats:sup>\n                      PD-1\n                      <jats:sup>+<\/jats:sup>\n                      CXCR5\n                      <jats:sup>\u2212<\/jats:sup>\n                      ICOS\n                      <jats:sup>+<\/jats:sup>\n                      kidney-derived Tph cells was higher in 16-week-old than in 8-week-old BXSB- Yaa and C57BL\/6 mice, whereas the frequency of CD4\n                      <jats:sup>+<\/jats:sup>\n                      PD-1\n                      <jats:sup>+<\/jats:sup>\n                      CXCR5\n                      <jats:sup>+<\/jats:sup>\n                      ICOS\n                      <jats:sup>+<\/jats:sup>\n                      kidney-derived T follicular helper (Tfh) cells was not significantly different between the mice. PD-L1 was constitutively expressed in the renal tubules. PD-L2 was expressed in the glomeruli of 16-week-old BXSB- Yaa mice. The frequency of PD-L1\n                      <jats:sup>high<\/jats:sup>\n                      CD11c\n                      <jats:sup>+<\/jats:sup>\n                      CD3\n                      <jats:sup>\u2212<\/jats:sup>\n                      CD19\n                      <jats:sup>-<\/jats:sup>\n                      and PD-L2\n                      <jats:sup>+<\/jats:sup>\n                      CD11c\n                      <jats:sup>+<\/jats:sup>\n                      CD3\n                      <jats:sup>\u2212<\/jats:sup>\n                      CD19\n                      <jats:sup>-<\/jats:sup>\n                      kidney-derived MNCs in 16-week-old BXSB- Yaa mice was significantly higher than that of the control mice. The percentage of kidney-derived Tph cells but not Tfh cells was correlated with the urinary protein levels in the nephritic mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      The results of this study suggest that kidney-infiltrating PD-1\n                      <jats:sup>+<\/jats:sup>\n                      Tph cells expanded concomitantly with the upregulation of PD-L1 and PD-L2 in the kidneys and the progression of lupus nephritis.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/09612033241247908","type":"journal-article","created":{"date-parts":[[2024,4,15]],"date-time":"2024-04-15T23:53:21Z","timestamp":1713225201000},"page":"816-827","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":2,"title":["Upregulation of PD-1 and its ligands and expansion of T peripheral helper cells in the nephritic kidneys of lupus-prone BXSB-\n                    <i>Yaa<\/i>\n                    mice"],"prefix":"10.1177","volume":"33","author":[{"given":"Rina","family":"Moriyama","sequence":"first","affiliation":[{"name":"Division of Rheumatology, Department of Internal Medicine, Tokyo Women\u2019s Medical University School of Medicine, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1654-0119","authenticated-orcid":false,"given":"Yasuhiro","family":"Katsumata","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Internal Medicine, Tokyo Women\u2019s Medical University School of Medicine, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuko","family":"Okamoto","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Internal Medicine, Tokyo Women\u2019s Medical University School of Medicine, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masayoshi","family":"Harigai","sequence":"additional","affiliation":[{"name":"Division of Rheumatology, Department of Internal Medicine, Tokyo Women\u2019s Medical University School of Medicine, Tokyo, 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